A major obstacle in the identification of disease-specific causal variants at TNFSF4 in the European and East Asian SLE cohorts has been the strong linkage disequilibrium (R2>0.8) exhibited by genotyped TNFSF4 alleles, which has resulted in a high frequency extended haplotype associated with risk of disease instead of delineating causal variations at the locus [4]. Here, TNFSF4 is linked to systemic lupus erythematosus.